Hyae Lim Min1, Jin Kim2, Woo Ho Kim3, Bo Gun Jang4, Min A Kim5. 1. Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea Department of Cancer Biology, Seoul National University College of Medicine, Seoul, Republic of Korea. 2. Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea Department of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea. 3. Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea Department of Cancer Biology, Seoul National University College of Medicine, Seoul, Republic of Korea Department of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea. 4. Department of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea. 5. Department of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea everest@snu.ac.kr.
Abstract
BACKGROUND: The metabolic enzyme, glycine dehydrogenase (GLDC), involved in glycine metabolism, is known to be involved in non-ketotic hyperglycinemia but not in cancer. Herein, we investigated GLDC expression and its promoter methylation in gastric cancer (GC). MATERIALS AND METHODS: GLDC expression and epigenetics were investigated using GC cell lines and tissues. Functional studies were also performed for identification of a correlation between methylated GLDC genes and gastric cancer progression. RESULTS: The results of the study can be summarized as follows: (i) GLDC was silenced in GC cell lines and tissues. The down-regulation of GLDC was closely linked to promoter methylation. (ii) Knockdown of GLDC increased cell proliferation, migration, invasion, colony formation and reduced apoptosis. (iii) In GC tissues, hypermethylation of GLDC had a significant correlation with down-regulation of the GLDC protein compared to normal gastric tissues. CONCLUSION: GLDC is a putative tumor suppressor gene involved in gastric cancer progression and hypermethylation of the GLDC promoter regulates its transcriptional silencing. Copyright
BACKGROUND: The metabolic enzyme, glycine dehydrogenase (GLDC), involved in glycine metabolism, is known to be involved in non-ketotic hyperglycinemia but not in cancer. Herein, we investigated GLDC expression and its promoter methylation in gastric cancer (GC). MATERIALS AND METHODS:GLDC expression and epigenetics were investigated using GC cell lines and tissues. Functional studies were also performed for identification of a correlation between methylated GLDC genes and gastric cancer progression. RESULTS: The results of the study can be summarized as follows: (i) GLDC was silenced in GC cell lines and tissues. The down-regulation of GLDC was closely linked to promoter methylation. (ii) Knockdown of GLDC increased cell proliferation, migration, invasion, colony formation and reduced apoptosis. (iii) In GC tissues, hypermethylation of GLDC had a significant correlation with down-regulation of the GLDC protein compared to normal gastric tissues. CONCLUSION:GLDC is a putative tumor suppressor gene involved in gastric cancer progression and hypermethylation of the GLDC promoter regulates its transcriptional silencing. Copyright
Authors: Samantha Goodman; Grace Chappell; Kathryn Z Guyton; Igor P Pogribny; Ivan Rusyn Journal: Mutat Res Rev Mutat Res Date: 2021-12-09 Impact factor: 7.015
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